Neurological disorders (for example, Parkinson's disease, Alzheimer's disease, polyglutamine diseases (Huntington's disease, spinocerebellar degeneration and the like), amyotrophic lateral sclerosis, polyneuropathy, spinal cord injury and cerebrovascular disease) occur as a result of degeneration, reduction or cell death of cerebral or peripheral neurons due to aging or environmental or genetic factors, or as a result of injury or removal. Effective treatments for such neurological disorders therefore include replenishment of neurotransmitters lost by the damaged neurons, or regeneration of the neurons. Sources of neurotransmitters include undifferentiated neural stem cells, and ES cells which are capable of differentiating to many different cell types.
However, because very few endogenous neural stem cells are capable of differentiating into nerves and it is not possible to sufficiently replenish cells that have degenerated due to cerebrovascular disease or the like, it is necessary to rely on external sources (specifically fetal neural stem cells or human ES cells), whereby ethical and transplantative antigenic problems may arise. Moreover, no techniques have been established for reliable differentiation into neurons, and their functions have not been successfully regenerated. In addition, regenerative medicine, which is concerned with regeneration of the central nervous system, has not been widely employed because of the problems inherent with its use of aborted fetal brains.
Recently, however, growth of new neurons (known as “neurogenesis”) in the hippocampus of adult brains has been reported. This has led to research toward methods for treating neurological disorders by stimulation of neural stem cells in the brains of patients, using drugs and the like, to induce their regeneration (for example, fibroblast growth factor-2 (Non-patent document 1) and NGF (Non-patent document 2)). However, since all such proteins or proteinaceous factors must be injected into the brain and are therefore difficult to employ for general medical treatment, low molecular compound substitutes for these proteins such as salvianolic acid B (Patent document 1) and lithium or its pharmacologically acceptable salts (Patent document 2) have been proposed.
Moreover, recently published reports describe confirmed augmentation of neurogenesis in the hippocampus when mother mice are loaded with taurine by oral administration, fetal mice are loaded via the breast milk, and neuronal development is observed by intraabdominal administration of BrdU (Non-patent document 3). In addition, it has been reported that administration of DHA (docosahexaenoic acid) to third-generation DHA-deficient aged rats promotes neurogenesis in the hippocampus (Non-patent document 4). A correlation has also been found between depression and reduced neurogenesis.
On the other hand, it has been demonstrated that arachidonic acid and/or compounds containing arachidonic acid as a constituent fatty acid improve symptoms of reduced brain function, and specifically, when aged animals are examined with a Morris water maze test, the reduced learning ability that accompanies aging is improved by administration of arachidonic acid and/or compounds containing arachidonic acid as a constituent fatty acid (Patent document 3).    Patent document 1: Japanese Unexamined Patent Publication No. 2006-76948    Patent document 2: International Patent Publication No. WO2004/91663    Patent document 3: Japanese Unexamined Patent Publication No. 2003-48831    Non-patent document 1: Pro. Nat. Acad. Sci. USA, 5874-5879 (2001)    Non-patent document 2: Cell, 110, 429 (2002)    Non-patent document 3: Program of the 173rd Meeting of the Essential Amino Acid Research Council, p. 1, 2003    Non-patent document 4: Neuroscience, 139, 991-997 (2006)